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2002 Abstracts

New Abstracts of interest from a MEDLINE search (colon OR colorectal) AND cancer. ENTERED next to an item means that item has been entered on the main pages of the website.

Last Updated: 3/29/02

  1. COX2
  2. Altmed
  3. Miscellaneous


COX-2

  • 3/29/02 Chemoprevention of gastrointestinal malignancies with nonsteroidal antiinflammatory drugs Cancer 2002 Feb 15;94(4):950-963 PMID: 11920463 In multiple studies, the chronic use of nonsteroidal antiinflammatory drugs (NSAIDs) has been associated with a decreased incidence of several types of gastrointestinal (GI) neoplasia. This effect may be mediated by one of several intracellular mechanisms, some of which involve the inhibition of the cyclooxygenase-2 (COX-2) isoenzyme. In multiple studies of colorectal carcinoma, chronic NSAID use has shown a protective effect, with the majority of studies demonstrating a 30-70% risk reduction associated with NSAID use

  • 3/24/02 Nonsteroidal anti-inflammatory drugs, apoptosis, and colon-cancer chemoprevention Lancet Oncol 2002 Mar;3(3):166-74 PMID: 11902503 Nonsteroidal anti-inflammatory drugs (NSAIDs) can inhibit colorectal tumorigenesis and are among the few agents known to be chemopreventive. Epidemiological studies and experiments with animals have shown that NSAIDs have powerful anticolorectal cancer properties, but the mechanism of these effects remains unclear. NSAIDs can inhibit neoplastic growth by inducing apoptosis in cancer cells; the way they do this is currently an area of intense investigation. The most well-characterised pharmacological feature of NSAIDs is their inhibition of the enzyme cyclo-oxygenase (COX), which catalyses the synthesis of prostaglandins. Several studies have shown that COX inhibition prevents cell proliferation and promotes apoptosis. The chemopreventive effects of NSAIDs are thought to occur via this pathway. Other observations indicate that NSAIDs also promote apoptosis through mechanisms that are independent of COX inhibition. This idea is supported by the finding that compounds that are structurally similar to NSAIDs, but do not inhibit COX, also have chemopreventive and proapoptotic properties. COX-dependent and COX-independent mechanisms of apoptosis induction are not mutually exclusive, and it is likely that both have a role in the biological activity of NSAIDs. Knowledge of how NSAIDs prevent neoplastic growth will greatly aid the design of better chemopreventive drugs and novel treatments for colorectal cancer.

  • 3/15/02 Cyclooxygenase-2 activity altered the cell-surface carbohydrate antigens on colon cancer cells and enhanced liver metastasis. Cancer Res 2002 Mar 1;62(5):1567-72 PMID: 11888937 Cyclooxygenase-2 (COX-2) was recently reported (M. Tsujii and R. N. DuBois, Cell, 83: 493-501, 1995) to affect the metastatic potential of cells. Previous studies (M. Fukuda, Cancer Res., 56: 2237-2244, 1996) indicated that sialyl Lewis antigen expression is correlated with hematogenous metastasis of colon cancer. In the present study, we investigated the interaction between COX-2 activity, expression of sialyl Lewis antigens, in vitro cancer cell adhesion to endothelial cells, and in vivo metastatic potential

  • 3/22/02 COX-2 inhibitors in cancer treatment and prevention, a recent development Anticancer Drugs 2002 Feb;13(2):127-37 PMID: 11901304 NSAIDs block endogenous prostaglandin synthesis through inhibition of cyclooxygenase (COX) enzymatic activity. COX-2, a key isoenzyme in conversion of arachidonic acid to prostaglandins, is inducible by various agents such as growth factors and tumor promoters, and is frequently overexpressed in various tumors. The contribution of COX-2 to carcinogenesis and the malignant phenotype of tumor cells has been thought to be related to its abilities to (i) increase production of prostaglandins, (ii) convert procarcinogens to carcinogens, (iii) inhibit apoptosis, (iv) promote angiogenesis, (v) modulate inflammation and immune function, and (vi) increase tumor cell invasiveness, although some studies indicated that NSAIDs have COX-2-independent effects

  • 3/22/02 Colorectal cancer prevention and treatment by inhibition of cyclooxygenase-2. Nature Rev Cancer 2001 Oct;1(1):11-21 PMID: 11900248 Population-based studies have established that long-term intake of non-steroidal anti-inflammatory drugs (NSAIDs), compounds that inhibit the enzymatic activity of cyclooxygenase (COX), reduces the relative risk for developing colorectal cancer. These studies led to the identification of a molecular target, COX-2, that is involved in tumour promotion during colorectal cancer progression. Recent studies in humans indicate that therapy with specific COX-2 inhibitors might be an effective approach to colorectal cancer prevention and treatment.

  • 3/22/02 Cyclo-oxygenase 2: a pharmacological target for the prevention of cancer. Lancet Oncol 2001 Sep;2(9):544-51 PMID: 11905709 Understanding the mechanisms underlying carcinogenesis provides insights that are necessary for the development of therapeutic strategies to prevent cancer. Chemoprevention--the use of drugs or natural substances to inhibit carcinogenesis - is an important and rapidly evolving aspect of cancer research. We discuss evidence that cyclooxygenase 2 (COX 2), an inducible form of the enzyme, is a potential pharmacological target to prevent cancer. Key data implicating a causal relation between increased activity of COX 2 and carcinogenesis and possible mechanisms of action of COX 2 in this context are covered. Importantly, selective COX 2 inhibitors appear to be safe enough in human beings to allow large-scale clinical testing in healthy people. Several chemoprevention trials using selective COX 2 inhibitors are underway

    Alternative Medicine

  • 3/15/02 Resveratrol Induces Growth Inhibition, S-phase Arrest, Apoptosis, and Changes in Biomarker Expression in Several Human Cancer Cell Lines Clin Cancer Res 2002 Mar;8(3):893-903 PMID: 11895924 CONCLUSIONS: These studies provide support for the use of resveratrol in chemoprevention and cancer therapy trials. Cyclin D1, cyclin B1, beta-catenin, and apoptotic index could be useful biomarkers to evaluate treatment efficacy.

  • 3/15/02 Vitamin E Succinate Is a Potent Novel Antineoplastic Agent with High Selectivity and Cooperativity with Tumor Necrosis Factor-related Apoptosis-inducing Ligand (Apo2 Ligand) in Vivo : Clin Cancer Res 2002 Mar;8(3):863-9 PMID: 11895920 alpha-Tocopheryl succinate (alpha-TOS), a redox-inactive analogue of vitamin E, is a strong inducer of apoptosis, whereas alpha-tocopherol (alpha-TOH) lacks apoptogenic activity (J.

  • 3/15/02 Mechanism of lovastatin-induced apoptosis in intestinal epithelial cells. Carcinogenesis 2002 Mar;23(3):521-528 PMID: 11895868 We earlier showed that lovastatin potentiated the chemopreventive effects of sulindac against colon neoplasia in a rodent model and augments apoptosis induced by 5-FU and cisplatin in human colon cancer cells. In the present study, we investigated effects of lovastatin in spontaneously immortalized rat intestinal epithelial cells, IEC-18 and their K-ras transformed clones. Lovastatin induced morphologic changes (cell rounding and detachment) and apoptosis that were not influenced by K-ras mutations

  • 3/22/02 Serum total gangliosides and TA90-IC levels: novel immunologic markers in colorectal cancer. Cancer J 2002 Jan-Feb;8(1):55-61 PMID: 11898807 CONCLUSIONS: We speculate that a multiple-marker analysis that combines CEA values with serum ganglioside and TA90-IC values may be more sensitive than CEA value alone for detecting colorectal cancer. The potential prognostic significance of TA90-IC status in advanced disease warrants further investigation.

  • 3/22/02 Olive-oil consumption and health: the possible role of antioxidants. Lancet Oncol 2000 Oct;1:107-12 PMID: 11905662 Epidemiological data show that the Mediterranean diet has significant protective effects against cancer and coronary heart disease. We present evidence that it is the unique profile of the phenolic fraction, along with high intakes of squalene and the monounsaturated fatty acid, oleic acid, which confer its health-promoting properties

  • 3/24/02 Cancer prevention by bovine lactoferrin and underlying mechanisms--a review of experimental and clinical studies. Biochem Cell Biol 2002;80(1):131-6 PMID: 11908637 In experimental studies, bovine lactoferrin (bLF) has been found to significantly inhibit colon, esophagus, lung, and bladder carcinogenesis in rats when administered orally in the post-initiation stage. Furthermore, concomitant administration with carcinogens resulted in inhibition of colon carcinogenesis

  • 3/24/02 Panax ginseng--a non-organ-specific cancer preventive? Lancet Oncol 2001 Jan;2(1):49-55 PMID: 11905620 One promising candidate with cancer-preventive effects that are not specific to any organ is Panax ginseng C A Meyer, a herb with a long medicinal history. Its protective influence against cancer has been shown by extensive preclinical and epidemiological studies, but these effects